{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T05:27:35Z","timestamp":1787030855848,"version":"build-2736575974"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2008,1,1]],"date-time":"2008-01-01T00:00:00Z","timestamp":1199145600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Of a number of mAbs made by immunization with sort-purified marginal zone (MZ) B cells, one was shown to recognize the mouse scavenger receptor CD36. Although CD36 is expressed by most resting MZ B cells and not by follicular and B1 B cells, it is rapidly induced on follicular B cells in vitro following TLR and CD40 stimulation. In response to T-independent and T-dependent Ag challenge, we found that CD36 was expressed on IgM+ plasma cells, but down-regulated on isotype-switched plasma cells in vivo. Although development, localization, and phenotype of MZ B cells in CD36\u2212\/\u2212 mice appeared normal, there was a minor block in the transitional stages of mature B cell development. In both primary and secondary Ab responses to heat-killed Streptococcus pneumoniae (R36A strain), both phosphoryl choline (PC)-specific IgM and IgG levels in CD36\u2212\/\u2212 mice were slightly reduced compared with wild-type mice. In addition, mice deficient in both TLR2 and CD36 produced significantly reduced levels of anti-PC IgG titers than those of single gene-deficient mice, suggesting that they may cooperate in an anti-PC Ab response. Collectively, these results show that CD36 does not affect the development of B cells, but modulates both primary and secondary anti-PC Ab responses during S. pneumoniae infection similarly to TLR2.<\/jats:p>","DOI":"10.4049\/jimmunol.180.1.230","type":"journal-article","created":{"date-parts":[[2014,4,11]],"date-time":"2014-04-11T00:13:32Z","timestamp":1397175212000},"page":"230-237","source":"Crossref","is-referenced-by-count":47,"title":["CD36 Is Differentially Expressed on B Cell Subsets during Development and in Responses to Antigen"],"prefix":"10.1093","volume":"180","author":[{"given":"Woong-Jai","family":"Won","sequence":"first","affiliation":[{"name":"Division of Developmental and Clinical Immunology, University of Alabama at Birmingham , Bikminghan AL 35294"},{"name":"Department of Microbiology, University of Alabama at Birmingham , Bikminghan AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin F","family":"Bachmann","sequence":"additional","affiliation":[{"name":"Cytos Biotechnology AG , Wagistr 25, Schlieren-Zurich ,","place":["Switzerland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John F","family":"Kearney","sequence":"additional","affiliation":[{"name":"Division of Developmental and Clinical Immunology, University of Alabama at Birmingham , Bikminghan AL 35294"},{"name":"Department of Microbiology, University of Alabama at Birmingham , Bikminghan AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2008,1,1]]},"reference":[{"key":"2025032610014160300_R1","first-page":"195","volume-title":"Curr. 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